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AVIS INTERRUPTION DE SERVICE / SERVICE INTERRUPTION NOTIFICATION :
Nous devons procéder à une opération d'entretien du serveur Papyrus qui nécessitera une courte interruption de service le mardi 20 mars 2018 à partir de 8h30 HAE. Nous prévoyons un arrêt du service pour une période approximative de une à deux heures. Merci de votre compréhension. / We must perform a Papyrus server maintenance operation that will require a short service interruption on Tuesday, March 20, 2018 starting at 8:30 am EDT. We are expecting approximately one to two hours of down time during the maintenance. Thank you for your understanding.

The ADP-ribosylation factors (ARFs) are small GTPases involved in vesicular transport, lipids synthesis and cytoskeleton remodelling. The isoforms 1 (ARF1) and 6 (ARF6) are the most studied. ARF1 is classically distributed at the Golgi apparatus whereas ARF6 is found at the plasma membrane and onto recycling endosomes. It was recently demonstrated that ARF6 is highly expressed and activated in several breast cancer cell lines and is associated with enhanced migration and invasiveness. However, the role of ARF1, in these biologicals processes necessary for metastasis formation, remains unclear.
In this study, we used MDA-MB-231 cells, an invasive breast cancer cell line, that expressed high levels of EGFR (Epidermal Growth Factor Receptor) to investigate the role of ARF1 in migration and proliferation. To further establish the role of ARF1 in cell migration, EMT and proliferation, we used two experimental approaches. First, we decreased endogenous ARF1 expression by RNA interference and second we overexpressed the dominant negative (ARF1T31N) and constitutively active (ARF1Q71L) ARF1 mutants, which mimick the inactive and active forms of ARF1, respectively. We demonstrated that depletion of ARF1 as well as overexpression of the inactive form of ARF1 blocked EGFR-mediated cell migration and proliferation by inhibiting the activation of PI3Kinase.
Moreover, we showed, using invasive and non invasive breast cancer cell lines, that ARF1 and both Cytohesin-1 and Cytohesin-2 are required for invasivness. Using similar approaches, we reported that inactivation of ARF1 in MDA-MB-231 cells promotes cell growth arrest associated to senescence program by regulating the function of the Retinoblastoma protein pRb.
Altogether, these findings demonstrate a physiological role for ARF1 in cell migration and proliferation. These two biologicals events are necessary for breast cancer progression.